H pylori strains expressing CagA and carrying the cag pathogenicity island induce an inflammatory response in the gastric mucosa greater than that induced by strains lacking the pathogenicity island.[47] In a large prospective study, Mayr et al[48] provided evidence that infection with CagA-positive H pylori strains significantly increases the risk of early atherosclerosis in carotid arteries. Here, S100A8 is linked to infection.